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metabolic Flashcards

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1
Q

In ethanol toxicity what will the patient present like?

A

withdrawl symptoms: tremor, tachycardia, HTN, malaise, nausea,DTs
physiologic tolerance, dependence

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2
Q

What are some direct effects of ethanol toxicity?

A

cerebellar vermis atrophy (ataxia)
loss of purkinje cells
Bergmann’s gliosis in cerebellum

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3
Q

What are some indirect effects of ethanol toxicity?

A

vitamin deficiency with Werniecke’s or Korsakoff
liver cirrhosis…hyperammonemia
…..hepatic encephalopathy
cerebral trauma

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4
Q

How is ethanol toxicity diagnosed?

A

clinical presentation and patient history (CAGE)

blood alcohol levels

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5
Q

What is the treatment for ethanol toxicity

A

avoid alcohol, disulfram to condition patient to abstain

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6
Q

What are some possible complications of ethanol toxicity?

A

Werniecke-Korsakoff, liver cirrhosis, hepatic encephalopathy

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7
Q

What cell is seen in increased levels in the cerbrocortical tissue in hepatic encephalopathy?

A

astrocytes(responsible for removing ammonia by converting to glutamine)
excess ammonia in systemic bc of hepatic resistance

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8
Q

What is the etiology of hepatic encephalopathy?

A

metabolic toxicity of the brain due to increased portosytemic shunt

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9
Q

What is associated with hepatic encephalopathy?

A

70% of patients with cirrhosis have subtle HE signs

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10
Q

What is the pathophysiology of HE?

A

1.increased hepatic resistance so portosystemic shunt
2.increased ammonia levels in brain and body
astrocytes damaged because of increased ammonia
3.astrocytes cannot convert ammonia to glutamine
AND
1.increased production of endogenous benzodiazepene…2.increased GABA content of brain

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11
Q

What is the presentation of HE?

A
  1. initially confused, derangement of consciousness, increased psychomotor activity
  2. eventually -drowsy, stupor, coma
    - asterixis: intermittent muscle contract when attempt postural fixation
    - focal or general seizure
    - grimace, suck, grasp reflex present
    - exaggerated DTR, asymmetric DTR
    - Babinski
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12
Q

What are some potential causes of subacute combined degeneration?

A

diet-starvation, eating disorder

exposure to NO gas

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13
Q

What is the presentation of subacute combined degeneration?

A
  1. paresthesia legs, hands, feet symmetrical diffuse
  2. ataxia
  3. pernicious anemia
    progresses to
  4. motor: spastic weakness diffused and symmetrical
  5. dementia
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14
Q

What can vitB12 deficiency present like?

A

spinal myelopathy

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15
Q

what is the etiology of subacute combined degeneration?

A

DC and LC of spinal cord are demylinated

motor is eventually demylinated too

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16
Q

what happens to myelin in subacute combined degeneration?

A

vacoulation
myelin is destroyed -astrocytosis
interstitial edema occurs because of osmotic change

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17
Q

What is the treatment for Subacute combined degeneration

A

vitB12

recovery may be reversible but if complete parapalegia then recovery is poor

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18
Q

what is the etiology of subacute combined degeneration?

A

cant absorb vit B12 across intestine wall

-effects on blood cell development and myelin

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19
Q

What are some causes of thiamine vit b1 def?

A 
starvation
dietary problems
hyperemesis
renal dialysis
cancer
AIDS
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20
Q

what type of neurodisease is vit B1 deficiency?

A

peripheral neuropathy

metabolic

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21
Q

what is the pathophysiology of thiamine deficiency?

A
  1. thiamine not coming from diet as it should
  2. thiamine is a cofactor needed to produce ATP
  3. osmotic potentials change
  4. hemorrhage and necrosis around 3rd ventricle structures
  5. macros infiltrate lesions
  6. lesions become cystic
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22
Q

What is the presentation of thiamine deficiency?

A

cardiopathy
peripheral neuropathy
encephalopathy
can develop into Wernieckes then develop further into Korsakoffs

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23
Q

What is the treatment for thiamine deficiency?

A

medical emergency, vit B1 supplements

Korsakoff’s may remain, all else is reversible

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24
Q

what population is likely to get thiamine deficiency?

A

alcholics

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25
What is the most common cause of Werniecke's and Korsakoff's syndrome?
alcholism | 3% of alcoholics have either
26
what are some causes of Werniecke/Korsakoff?
similar to thiamine def. | hyperemesis, starvation, eating disorders, renal dialysis, AIDS, cancer
27
What is the pathophysiology of Werniecke/Korsakoff?
thiamine needed at cofactor for ATP production hermmorage and lesion around 3rd ventricle structures (hypothal, thal, mammilary bodies, colliculi), infiltrate with macros, lesion turns cystic (same as vit B1 thiamine def) leads to memory loss, confusion, ataxia
28
What is the presentaiton of Werniecke's syndrome?
confusion, opthalmopelgia (lateral rectus or lateral gaze) and gait ataxia
29
What is the presentation of Korsakoff's?
confabulation, memory loss (learning and retention) | can progress from Werniecke's
30
How is werniecke's and Korsakoff's diagnosed?
MRI: should see widening of 3rd ventricle and atrophy of paraventricular thalamus vestibular testing CAGE screen for alcholics
31
How is Werniecke's and Korsakoff's treated?
medical emergency thiamine avoid alcohol recovery from Korsakoff's might not happen
32
What are some complications to think about in Werniecke or Korsakoff's syndromes?
liver failure systemic infection ethanol toxicity alcohol withdrawal
33
what is the etiology of Wilson's?
genetic mutation of ATP7B gene autosomal recessive Cu transport ATPase protein defect
34
What is the presentation of Wilson's?
1.behavioral disturbance may present first 2.yellow green ring around cornea 3.liver signs autonomic:BB incontinence, sweating, orthostatic hypotension 4.BG signs: dystonia, tremor, incoordination dementia migraine, seizure
35
where does the Cu accumulate since it cannot be transported in Wilson's disease?
liver and basal ganglia
36
What is the treatment for Wilson's
``` chelating agent -penicillamine liver transplant (curative) ```
37
How is Wilson's diagnosed?
1. low serum ceruplasmin (protein that carries Cu in blood) 2. eye rings 3. MRI lesions high intensity on T2 (cell loss and gliosis) 4. Cu toxicity in tissue 5. genetic test
38
What is the pathophysiology of Wilson's?
1. mutation in ATPB7 gene 2. no ATPase to transport Cu 3. failure at biliary excretion of CU 3. Cu accumulate in BG and liver 4. BG: dementia, tremor, incoordination 5. Hepatic: hepatitis, cirrhosis, failure
39
what increases the liklihood of Wilsons?
co-sanguinous populations US heterozygote carrier 1/100 Japan has higher incidence
40
what are some complications to think about in Wilson's?
higher rate of natural abortions during pregnancy can develop Werniecke-Korsakoff liver cirrhosis, hepatic encephalopahty
41
what type of neuropathy is diabetic neuropathy?
metabolic sensorineural peripheral
42
What is the most common cause of peripheral neuropathy worldwide?
diabetic neuropathy
43
What some metabolic sensorineural neuropathies?
Diabetic (chronic only becomes motor) (lose pain) Thiamine Thallium Cisplastin (pain preserved) (vit B12 subactute combined degen mostly sensory much later can become motor)
44
After 25 years with diabetes, what percentage have diabetic neuropathy?
50% upon diagnosis, 8% have some subtle signs 6.5% prevalence in US
45
What are the 4 pathways believed to be involved in diabetic neuropathy?
polyol pathway increase hexoamine pathway increase glycolation pathway increase PKC increase activity so more proinflamm 1. leads to increase in free radicals and decrease in scavengers 2. Vascular insufficiency
46
What is the etiology of diabetic neuropathy
- metabolic uncontrolled glucose levels - vascular insufficiency so lose of small fibers - and segmental demylination-axonopathy
47
what are some rare presentations of diabetic neuropathy?
autonomic focal or multifocal asymm neuropathy small fiber and painful neuropathy regional neuropathic syndrome
48
What are the signs of classic diabetic neuropathy?
sensorineural peripheral 1. numb tingle painless distal extremities 2. pain worse at night begins in toes then up to calves then fingers and then arms 3. chronic: motor weakness distal and atrophy 4. chronic decreased DTRs 5. sometimes autonomic dysfunction
49
How is diabetic neuropathy diagnosed?
clincial findings, conduction studies not definitive, biopsy not usually
50
what are some complications to think about with diabetic neuropathy?
``` pain control: TCA, tramadol, anticonvulsants, narcotics foot ulceration (foot hygiene) ```
51
what is the treatment for diabetic neuropahty?
``` none really (manage blood levels glucose) free rad scavengers not very helpful ```
52
what is the presentation of cisplatin neuropathy?
1. lose 2 PV 2. pain retained 3. paresthesia extremities 4. lose hair cells
53
What type of neuropathy is cause by cisplatin?
sensorineural metabolic peripheral
54
what is the pathophysiology of cistplatin neuropathy?
axon degeneration | kills DRG in does dependent manner
55
what is the most common toxic neuropathy in the US?
anticancer drugs like cistplatin
56
what is the temporal profile of alcohol neuropathy?
progressive slow
57
what type of neuropathy is alcohol neuropathy?
peripheral sensorimotor
58
what are some common sensorimotor peripheral neuropathies?
alcohol, Hg, Arsenic, thiamine (vitb12 starts out sensory but can progress to motor) (diabetic starts sensory but chronic can become motor)
59
What are some common motor peripheral neuropathies?
Pb
60
What is the presentation of alcoholic neuropathy?
1. burning paresthesias 2. painful cramps 3. weakness, wasting Stocking glove pattern for impaired 2 PV and PT
61
What is the most common heavy metal neuropathy?
arsenic
62
What is the pathophys of alcholic neuropathy
demylination axonopathy remits with abstinence
63
What are some common presentations of heavy metal peripheral neuropathies?
encephalopathy, peripheral neuropathy
64
How does lead heavy metal neuropahty present?
motor neuropathy 1. UE weak> LE weak 2. distal symmetric 3. late stage-autonomic involvement
65
how does mercury heavy metal neuropathy present?
sensorimotor 1. exposure: industrial, dietary, dental amalgam 2. distal
66
How does thallium heavy metal neuropahty present?
sensorineural 1. exposure: pesticides, rodenticides, industria, diet 2. distal, symmetric 3. mostly sensory large fibers 2PV axonopathy 4. late state-autonomic
67
how does arsenic heavy metal neuropathy present?
sensorimotor. slow onset 1. exposure: drinking water, intentional, industrial 2. symm 3. burning paresthesias initially 4. LE weakness> UE weakness 5. lose DTRs
68
Which toxic metals cause axonopathy?
thallium, Arsenic, cisplatin, thiamine | alcohol also does
69
How can you differentiate alcoholic neuropathy and arsenic heavy metal?
both are burning, both are sensorimotor, both progressive slow onset arsenic presents with LE weakness greater than Upper extremity. lose DTRS alcholic presents with stocking glove paresthesia and painful cramps
70
What is the temporal profile of arsenic neuropathy?
slow progressive
71
What are the signs and symptoms of Thiamine B1 deficiency?
cardiopathy encephalopathy W andK neuropathy-sensorimotor
72
What is the presentation of thiamine B1 neuropathy?
sensorimotor 1. acute, subacute onset 2. paresthesia stocking glove 3. weakness in legs 4. Lose DTRS
73
How is thiamine deficiency diagnosed?
empiric threatment with oral Thiamine B1
74
In a long standing alcoholic patient what would be found in cerbellum?
dead purkinje cells | Bergmann's gliosis because glial cells proliferate due to dead purkinje cells
75
On imaging of a Werniecke-Korsakoff patient what would you see?
widening of 3rd ventricle | atrophy of paraventricular thalamus
76
What is a demylinating disease of the pons?
central pontine myelinolysis
77
What patient population is likely to get CPM?
liver transplant alcoholics (1/2 of cases) renal dialysis
78
what is the etiology of CPM?
rapid over correct for hyponatremia
79
what is the presentation of CPM?
1. acute to subacute 2. loss of ability to use cranial nerves (can't chew, swallow, speak) 3. flaccid paralysis all 4 limbs
80
What might be spared in CPM?
ocular movements and facial movements (pons and midbrain) | "locked in syndrome"

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